Neurology News

Migraine is one of the most incapacitating conditions, affecting one in every seven persons and posing a significant social and economic cost. Several studies have found that migraine is a condition that affects a broad area of the central nervous system and is defined by a systemic failure in sensory information processing and integration that occurs even between migraine episodes (interictal period). Patients with migraine, for example, have enhanced cerebral reactions to sensory inputs during the interictal interval. At the moment, the biological processes causing these changes are mainly unclear.

A team of neuroscientists led by Mirko Santello at the University of Zurich’s Institute of Pharmacology and Toxicology, in conjunction with the University of Padua, has found a novel mechanism linked in a rare form of migraine caused by genetic mutation. They claim that this familial hemiplegic migraine type 2 (FHM2) causes astrocytes in the cingulate cortex, a brain area implicated in pain perception, to fail. Astrocytes, or star-shaped brain cells, are critical contributors to neuronal function and have a significant influence on brain circuits and behaviour.

“Despite their abundance, astrocytes have been relatively overlooked by neuroscientists,” says Mirko Santello, last author of the study. Nonetheless, these cells are critical in clearing neurotransmitters. The researchers were able to demonstrate that in familial migraine, astrocytes are unable to eliminate excessive transmitters generated by neurons.

“The impairment in astrocytic glutamate uptake in the cingulate cortex strongly enhances cortical dendritic excitability and thus enhances firing of the neurons,” Santello says. Furthermore, the study found that cingulate brain dysfunction impacts migraine incidence. The researchers demonstrated greater sensitivity to head pain triggers in a mouse model.

“By manipulating astrocytes in the cingulate cortex, we were able to reverse their dysfunction. This prevented an increase in head pain in mice carrying the genetic defect,” says Jennifer Romanos, first author of the study. Migraine is a complex neurological illness that affects a portion of the nerve system.

“Our results provide a clear example of how astrocyte dysfunction produced by a genetic defect affects neuronal activity and sensitivity to head pain triggers,” explains Mirko Santello. The findings contribute to a better understanding of migraine pathogenesis and imply that the cingulate cortex is a major hub in the condition. The discovery of a relationship between astrocyte malfunction in the cingulate cortex and familial migraine may aid in the development of novel migraine treatment techniques.

Ludwig Cancer Research team have found a single protein that is produced at high levels by cancer cells across a wide spectrum of malignancies. In animal models of cancer, this protein builds a complex barrier to anti-cancer immune responses, shielding tumours from immune identification and killing.

The study, led by Douglas Hanahan of Ludwig Lausanne, Qiqun Zeng and Sadegh Saghafinia, both former members of his lab, and graduate student Agnieszka Chryplewicz, also outlines a signature of gene expression induced by the protein, known as FMRP, that encompasses 156 different genes and predicts poor patient survival in a variety of cancer types.

The findings, published in the journal Science, might help guide the selection of patients who will benefit from immunotherapies and the development of novel medicines for a variety of cancers in the future.

“Our study has detailed a previously unknown and apparently common mechanism by which malignant cells shut down anti-cancer immune responses,” said Hanahan, a distinguished scholar at the Ludwig Institute for Cancer Research Lausanne Branch.

“We have shown that the hyperexpression of FMRP, which we and others have previously linked to tumour progression, doesn’t directly drive cancer cell proliferation and tumour growth. Rather, it supports the ability of malignant cells to manipulate the types and functional states of immune cells around them in a manner that very effectively subverts immune attack.”

Fragile X syndrome, a neurodevelopmental disorder that causes severe intellectual impairment, has been related to FMRP, a protein that is mostly synthesised in neurons and is being studied as a possible risk factor. FMRP is a protein that controls gene-to-protein translation and assists in the stabilisation of messenger RNA readouts in cells. However, its role in the genesis of cancer remained unclear.

The researchers began by establishing that greater FMRP levels may be seen in a range of tumour types. In order to examine the role of FMRP in cancer, they employed CRISPR-Cas9 gene editing to eliminate FMR1, the gene that encodes FMRP, from mouse cancer cell lines.

They constructed mouse models of pancreatic, colon, melanoma, and breast tumours using the changed cell lines and compared them to equivalent tumours that retained their FMR1 genes using animals with or without intact immune systems.

All tumours expanded evenly in culture and in immunocompromised animals, but those missing the FMR1 gene grew at a significantly slower rate in mice with functional immune systems. They were also densely packed with cytotoxic and helper T cells, both of which are critical for the immune system’s capacity to combat cancer. Tumors with intact FMR1 genes, on the other hand, progressed swiftly and lacked anti-tumor T cells, gaining the term “immune deserts.”

When T cells were removed from FMR1-deficient tumours, they stopped growing, demonstrating that FMRP promotes tumour growth via modulating the immune response.

The FMRP-regulated gene-expression pathway in cancer cells activates a range of immune evasion-supporting defence mechanisms, according to the researchers.

One of these is the release of substances that, among other things, promote the induction of regulatory T cells, inhibit the activity of cytotoxic T cells, or rewire immune cells known as macrophages so that they support the growth and survival of cancer cells rather than destroying them, primarily through the pacification of T cells.

The lack of FMRP in cancer cells, on the other hand, resulted in the reversal of their immunosuppressive effects as well as the production of a chemical that attracts T lymphocytes.

The FMRP-deficient cancer cells also produced signals that instructed tumor-infiltrating macrophages to engage in a stimulatory programme that aided in the recruitment and activation of T cells capable of eliminating the tumour.
Despite the fact that FMRP expression alone is not a good predictive biomarker for cancer outcomes, the researchers reveal that a gene expression profile representing the regulatory network it produces accurately predicts relatively low survival probabilities in a range of cancer types.

“We are hopeful that these discoveries can be translated into diagnostics and therapies of benefit to cancer patients, as the hallmark capability of cancers to circumvent immune responses underlies the resistance of many tumour types to immunotherapy,” said Hanahan.

To that end, the researchers founded Opna Bio, which is researching cancer therapies that target FMRP and the mechanisms via which it works

The protein medin, like the protein amyloid-, accumulates in the blood vessels of Alzheimer’s patients’ brains. DZNE researchers discovered this ‘co-aggregation.’ Their discovery has subsequently been published in the prestigious journal Nature.

“Although Medin has been around for more than 20 years, its impact on illnesses was previously underrated. We were able to demonstrate that medin considerably increases the pathological changes in the blood vessels of Alzheimer’s patients “explains Dr Jonas Neher, the study’s principal investigator and director of the DZNE’s Tubingen location.

The University of Tubingen, the Hertie Institute for Clinical Brain Research in Tubingen, and a variety of international organisations and cooperation partners all contributed to this extensive study. Amyloid is exemplified by Medin. The most well-known of these proteins is amyloid-, which clumps in the brains of Alzheimer’s patients. The brain’s blood arteries and tissue are both injured as a result of these aggregates’ eventual deposition as plaques, which in turn destroy the brain’s nerve cells and blood vessels.

But while amyloid- has been the subject of numerous investigations, medin has not drawn much attention. Jonas Neher notes that “there was minimal evidence of pathology, that is, of a clinically noteworthy finding connected with medin,” and that “pathology is frequently the prerequisite for a more in-depth research of an amyloid.”

Medin, on the other hand, is the most common amyloid and may be found in the blood vessels of nearly everyone over the age of 50. Jonas Neher and his colleagues discovered that medin appears in old mice and published their findings in the scientific journal PNAS two years ago.
It was revealed at the time that medin accumulated more in the mice’s brain blood vessels as they matured.

Furthermore, as the brain becomes active and blood flow increases, medin-deposited blood vessels expand more slowly than medin-free blood vessels. However, the capacity of blood vessels to develop is critical for providing the brain with adequate oxygen and nutrients.

On top of that, the researchers’ most recent studies focused on Alzheimer’s disease. First, scientists were able to show in Alzheimer’s mouse models that the presence of amyloid deposits leads medin to accumulate substantially more strongly in the blood arteries of the brain.

Importantly, the study of brain tissue from organ donors with Alzheimer’s disease validated these findings. However, far fewer amyloid- deposits accumulated in mice whose genes were changed to prevent the production of medin, resulting in fewer blood vessel damage.

“There are only a handful of research groups worldwide working on medin at all,” says Jonas Neher. A recent study from the United States found that medin levels may rise in Alzheimer’s sufferers. However, it was unclear if this rise was simply a result of the sickness or if it was one of the reasons.

“We have now been able to show through many experiments that medin actually promotes vascular pathology in Alzheimer’s models,” Neher said. So medin deposits are indeed a cause of blood vessel damage. “And this indicates that medin is one of the causes of the disease,” Neher said.

The scientists employed tissue pieces from mice and Alzheimer’s patients that had been coloured so that certain proteins could be detected in their study. They were able to show that medin and amyloid- are co-localized, or deposited together, in the blood vessels of the brain. They were able to show that these two amyloids co-aggregate, or form mixed deposits, in a later stage.

According to Jonas Neher, the findings “amazingly, medin interacts directly with amyloid- and enhances its aggregation – which was entirely unknown.” This realisation has given the researchers hope for the development of a revolutionary therapy.

As a result of amyloid buildup in the brain’s blood vessels, they suggest that Medin “may be a therapeutic target to avoid vascular injury and cognitive decline.”

Alzheimer’s disease is undoubtedly facilitated by vascular alterations, impaired function, or damage to blood vessels, as well as amyloid-aggregates in brain tissue. Patients may benefit from medicines that target both damaged blood vessels and plaques.

The next phase will be to see if medin aggregates can be eliminated therapeutically and, if so, whether this intervention ha any effect on cognitive performance. The researchers intend to test this in mice initially since animal models properly replicate the pathogenic changes in Alzheimer’s sufferers.

A new study at the California Institute of Technology demonstrates how devices implanted into people’s brains have the ability to precisely detect which phrases a tetraplegic participant was just thinking rather than speaking or miming.
“Online internal speech decoding from single neurons in a human participant,” a novel discovery, was presented at the 2022 Society for Neuroscience conference in San Diego. The researchers used the opportunity to show off their brain-machine interfaces (BMIs), which might eventually help speech-impaired patients.

“You may already have seen videos of people with tetraplegia using BMIs to control robotic arms and hands, for example to grab a bottle and to drink from it or to eat a piece of chocolate,” says Sarah Wandelt, a Caltech graduate student in the lab of Richard Andersen, James G. Boswell Professor of Neuroscience and director of the Tianqiao and Chrissy Chen Brain-Machine Interface Center at Caltech.

“These new results are promising in the areas of language and communication. We used a BMI to reconstruct speech,” says Wandelt, who presented the results at the conference on November 13.

Previous research has found that examining brain signals captured from motor regions when a participant whispered or mimed phrases can help anticipate participants’ speech. Internal communication, on the other hand, is far more difficult to foresee since it does not entail any movement, argues Wandelt. “In the past, algorithms that tried to predict internal speech have only been able to predict three or four words and with low accuracy or not in real time,” Wandelt says.

The current study is the most accurate at predicting internal words yet. Brain signals were collected from single neurons in the supramarginal gyrus, which is located in the posterior parietal cortex. In a prior study, the researchers discovered that this brain region represented spoken words.

The team has now expanded their results to include internal speech. The researchers then taught the BMI gadget to distinguish the brain signals produced when the tetraplegic subject talked internally or thought particular phrases. This training session lasted roughly 15 minutes. They then displayed a word on a screen and instructed the participant to speak it internally.

The results indicated that the BMI algorithms could identify eight words with up to 91 percent accuracy.
The research is still in its early stages, but it might benefit people with brain injuries, paralysis, or disorders that impact speech, such as amyotrophic lateral sclerosis (ALS).

“Neurological disorders can lead to complete paralysis of voluntary muscles, resulting in patients being unable to speak or move, but they are still able to think and reason. For that population, an internal speech BMI would be incredibly helpful,” Wandelt says.

“We have previously shown that we can decode imagined hand shapes for grasping from the human supramarginal gyrus,” says Andersen. “Being able to also decode speech from this area suggests that one implant can recover two important human abilities: grasping and speech.”

The researchers also point out that BMIs cannot be used to read people’s minds since the device would have to be trained in each person’s brain independently, and they only operate when the person concentrates on the word.

The National Institutes of Health, the Tianqiao and Chrissy Chen Brain-Machine Interface Center, and the Boswell Foundation financed the study, which is now being peer reviewed but has not yet been published. Aside from Wandelt and Andersen, other Caltech contributors include David Bjanes, Kelsie Pejsa, Brian Lee (PhD ’06), and Charles Liu. Lee and Liu are Caltech visiting associates who also teach at USC’s Keck School of Medicine.

A recent study from the University of South California demonstrates that a specific pattern of white matter connectivity has been found in the brains of autistic people. It is also distinct from the pattern seen in those with Developmental Coordination Disorder (DCD).

According to the study, which was published in the journal ‘Scientific Reports,’ roughly 85 percent of autistic persons have had or are at risk of being diagnosed with DCD, a disorder that interferes with learning and motor control. DCD can impede daily tasks such as typing, dressing, and walking, reducing one’s social involvement and enjoyment.

Distinguishing between the brain activity patterns of autism spectrum disorder (ASD) and DCD populations is critical because the widespread comorbidity of ASD and DCD confounds previous autism research, which was thought to be exclusively investigating its core social-communication symptoms at the time it was conducted.

“As the scientific community has learned more about DCD, we realised that white matter disparities previously observed in the autism literature might really be attributable to this underlying motor comorbidity,” stated senior author Lisa Aziz-Zadeh. “In reality, that’s exactly what our team discovered: many earlier research findings are likely not representing autism’s core symptoms, but rather co-occurring DCD.”

Aziz-Zadeh is an associate professor in the USC Dornsife College of Letters, Arts, and Sciences’ Brain and Creativity Institute and the Department of Psychology. She is the director of the USC Center for the Neuroscience of Embodied Cognition, which manages research projects funded by the National Institutes of Health, the US Department of Defense, and the Intelligence Advanced Research Projects Activity of the Office of the Director of National Intelligence.
Aziz-Zadeh and colleagues employed diffusion weighted MRI, a method for evaluating functional brain connections, on children and teenagers aged 8 to 17 years old who were randomly allocated to one of three research groups: those with ASD, those with suspected DCD, and those who were normally developing.

The photos were evaluated, compared, and connected with physical and social behaviour assessments performed by the participants. The researchers discovered that numerous structural brain connection patterns previously associated with autism also overlap with DCD. The team was able to identify three white matter pathways with distinctly different connectivity, distinct from the DCD and typically developing groups: the longitudinal fibres and u-fibers of the mid-cingulum, the corpus callosum forceps minor/anterior commissure, and the left middle cerebellar peduncle. These disparities were also connected to autistic participants’ emotional performance and/or autism severity. Children with DCD had distinct white matter patterns in the left cortico-spinal and cortico-pontine tracts.

“These findings show that we can use advanced imaging to differentiate between autism’s hallmark social symptoms and other motor-related symptoms at the level of brain anatomy,” said Emily Kilroy, the study’s first author and a former postdoctoral scholar in Aziz-lab Zadeh’s during the data collection period. “Of course, people are much more than their brain structure,” says the researcher, “but this level of clarity and precision at the anatomical level brings us one step closer to understanding the molecular foundation and presentation of autism.”

Researchers have found one of the causes of neuroblastoma’s resistance to treatment. The findings have ramifications for how future therapies should be created. The research was undertaken by Lund University in Sweden, and the results were reported in Science Advances. Neuroblastoma is a deadly cancer of the sympathetic nervous system, particularly the adrenal gland. Despite intensive chemotherapy treatment, the disease can be difficult to cure, and the prognosis for children with the aggressive type is bleak. One of the causes is that the tumour frequently develops medication resistance.

In order to understand what happens when the tumour becomes resistant, good disease models are needed that can mimic the complex drug treatment given to patients today:
“Tumours from patients with neuroblastoma look very different, and it is difficult to produce a model that is representative of many patients. This type of challenge often limits medical research”, explains the study’s first author, Adriana Manas, child cancer researcher at Lund University.

However, the researchers have now succeeded in building a model in mice using human neuroblastoma tumour cells, allowing them to track the pathways that occur when particular tumour cells gain treatment resistance. “What happens is that the tumour cells change to mimic embryonic cells from the fetal development phase. These embryonic tumour cells are more resistant to chemotherapy”, says research group leader Daniel Bexell, who led the study.

It has long been recognised that genetic alterations are required for neuroblastoma to originate and progress into an aggressive tumour. When it comes to resistance, however, it is not so much about genetic alterations as it is about cells swiftly adapting their behaviour. The researchers believe that the cells in their young form can adapt and survive in changing environments, which is why embryonic tumour cells are less susceptible to treatments.

“Current treatment with chemotherapy targets rapidly dividing tumour cells. Our research results can contribute to new treatments which better reach the entire tumour, in order to avoid the development of resistance. In future research, it will be important to understand how to specifically target the embryonic state of the neuroblastoma cell in order to cure patients”, concluded Daniel Bexell.

A team of USC Keck School of Medicine researchers conducted the first documented study of the brains of boys and girls with binge eating disorder and observed significant differences in brain anatomy between the sexes.
The findings were just published in the journal Psychological Medicine. The study, which builds on previous research suggesting that binge eating disorder is hardwired in the brain from birth, is an important first step toward understanding the neurobiology of binge eating disorder and how it differs between sexes.

It also provides vital evidence that boys, who were previously excluded from eating disorder studies, must be included in future efforts to understand the genesis of eating disorders. “Males have been excluded from eating disorder research for decades,” said Stuart Murray, DClinPsych, PhD, Della Martin Associate Professor of Psychiatry and the Behavioral Sciences at USC’s Keck School of Medicine, noting that the exclusion was perpetuated by the belief that eating disorders were uncommon in men. “As a result of the exclusion of boys and men, we have created therapies only via research on females, which we then apply to boys and men in the hope that they work as well.”

However, it has been increasingly obvious in recent years that some eating disorders are almost as common in men and boys as they are in women and girls. At the same time, research has shown increasing evidence that eating disorders are brain illnesses rather than the consequence of societal pressure or a lack of willpower, which Murray described as popular misconceptions that have been debunked.

The condition is the same, but the brain anatomy is different. Using data from the Adolescent Brain Cognitive Development project, the biggest brain development study in the United States, the researchers selected 38 boys and 33 girls among the study’s 11,875 participants who had a diagnosis of binge eating disorder. Boys account for around 57% of children with binge eating disorder.

Adult males account for around 43% of people suffering from binge eating disorders. Using voxel-based morphometry, a neuroimaging technique that allows researchers to assess variations in structural brain architecture throughout the whole brain, the research team was able to measure the grey matter density in the brains of the nine- and 10-year-olds in the study. It discovered that, when compared to a control group of 74 children who were age, BMI, and developmental maturity matched, girls with binge eating disorder had higher grey matter density in numerous areas of the brain known to be associated with impulse control and binge eating disorder symptoms. Boys with binge eating disorder, on the other hand, did not have increased grey matter density in these locations.

This increased grey matter density in binge eating disorder girls shows that a critical brain maturational process, synaptic pruning, may be disrupted or delayed in these girls.
“This data definitely indicates that any neurobiological explanation of binge eating disorder must be stratified by gender,” Murray added. Male inclusion is crucial for future therapies. Similarly, because boys and girls with binge eating disorder, the most frequent kind of eating problem, have distinct brain architecture, males may require different sorts of therapy than females. Murray also mentioned that novel therapies for binge eating disorder are on the way, including transcranial magnetic stimulation and direct current stimulation, both of which target the brain directly.

As with past studies on eating disorders, only female patients have been included in this study thus far.
“Because of the variations in brain anatomy between boys and girls with binge eating disorders, any therapy targeting the brain must be studied on both males and females,” Murray said. “Or else, we’d be targeting regions of the male brain that aren’t necessarily dysfunctional.” Murray and his colleagues will then investigate if, in addition to having distinct architecture, male and female binge eating disorder brains work differently.

Major cultural and political events, according to study, can have a considerable influence on psychological health, as well as sleep and emotional well-being. While popular belief says that highly anticipated events, such as elections, can generate stress and disturb well-being.
Researchers at Beth Israel Deaconess Medical Center (BIDMC) and colleagues have now demonstrated how large geopolitical events may have worldwide effects on sleep, which are related with considerable swings in the public’s collective mood, well-being, and alcohol use. The findings, published in the journal Sleep Health of the National Sleep Foundation, demonstrate that polarising political events had a detrimental impact on a wide range of characteristics associated to public mood.

“Given the political turmoil of the previous several years, it is doubtful that these findings would come as a surprise to many,” said corresponding author Tony Cunningham, PhD, director of BIDMC’s Center for Sleep and Cognition. “Our findings are likely to reflect many of our personal experiences in the aftermath of extremely stressful situations, and we saw this as an opportunity to empirically test these ideas.”

The team surveyed 437 participants in the United States and 106 international participants daily between October 1-13, 2020 (before the election) and October 30-November 12, 2020 (after the election) as part of a larger study investigating the sleep and psychological consequences of the COVID-19 pandemic (days surrounding the November 3 U.S. election). Participants reported on their sleep length and quality, alcohol intake, and subjective overall stress experience. Their replies demonstrated decreased sleep quantity and efficiency, as well as increased stress, bad mood, and alcohol consumption in the run-up to the election. While similar findings were seen at a lesser level in non-US participants, deteriorating health practises were only shown to be substantially linked with mood and stress among US residents.

The daily surveys, which were given each morning at 8:00 a.m. local time, asked respondents to evaluate the previous night’s sleep by documenting their bedtimes, time necessary to fall asleep, number of awakenings during the night, morning wake time, and time spent napping during the day. They also noted the prior night’s alcohol consumption. Mood was measured using a validated questionnaire as well as questions from a common depression screening instrument.
In terms of sleep, both US and non-US participants reported losing sleep in the run-up to the election; however, US respondents spent much less time in bed in the days before the election. On Election Night, participants in the United States reported waking up often during the night and having worse sleep efficiency.

Participants in the United States who had previously reported consuming alcohol increased their intake on three occasions throughout the evaluation period: Halloween, Election Day, and the day the election was declared by additional media sources, Saturday, November 7. There was no change in alcohol intake among non-US participants over the November evaluation period.
When the researchers examined how these behavioural changes may have influenced the mood and well-being of US individuals, they discovered substantial correlations between sleep and drinking, stress, bad mood, and depression.
The analysis found that stress levels for both U.S. and non-U.S. participants were relatively similar during the assessment period in early October, but there was a substantial increase in reported stress for both groups in the days running up to the November 3 election.

When the election was officially called on November 7, stress levels reduced considerably. This pattern remained true for both US and non-US residents, however changes in stress levels were much higher among US individuals.
Individuals in the United States observed a similar pattern with depression that their counterparts in other countries did not; nonetheless, non-U.S. participants showed substantial declines in negative mood and depression the day after the election was called.
“This is the first study to establish a link between previously observed variations in Election Day public mood and sleep on election night,” Cunningham said. “Moreover, data shows that sleep may impact civic engagement and participation in elections, as well as elections themselves.”

Thus, if the association between sleep and elections is indeed bidirectional, future study will need to understand how public mood and stress impacts on sleep before to an election may affect or even change its outcome.”
The authors caution that the interpretation of their findings is constrained because the bulk of participants’ experience was the accumulation of election stress and subsequent response reliant on their favourite political candidate. More study with a more representative and varied sample is required to confirm the effects of political stress on general public mood and sleep.

Trauma can result in dissociative symptoms such as an out-of-body experience or a sense of emotional numbness, which can be beneficial in the short term but harmful if they continue over an extended length of time.
McLean Hospital, the biggest psychiatric affiliate of Harvard Medical School and a component of Mass General Brigham, has uncovered locations within brain networks that communicate with one another when persons suffer dissociative symptoms. Their findings were published in the journal Neuropsychopharmacology recently.

“Dissociation and severe dissociative disorders like dissociative identity disorder or ‘DID’ remain at best unappreciated and, at worst, routinely go untreated or misdiagnosed,” said co-lead author and head of the Dissociative Disorders and Trauma Research Program Lauren A.M. Lebois, PhD.
“The cost of stigma and misdiagnosis is high: it has stopped people from receiving adequate and effective treatment, has caused extended suffering, and has stifled dissociation research. Furthermore, because DID affects women disproportionately, gender imbalance is a relevant issue in this setting.”
The study included 91 women with and without a history of childhood trauma, present post-traumatic stress disorder, and varied degrees of dissociative symptoms.

Participants underwent a functional magnetic resonance imaging scan so that researchers could learn more about their brain activity.
“The unique approaches we employed to analyse brain connections are crucial for understanding the role these network disruptions play in dissociative disorders,” stated co-senior author Lisa D. Nickerson, PhD, head of McLean Hospital’s Applied Neuroimaging Statistics Lab.
The researchers revealed that particular dissociation symptoms were linked to specific connections in the brain networks that govern cognitive and emotional processes. “We observed that dissociation important to DID and dissociation common to post-traumatic stress disorder are separately connected to unique brain signatures,” Lebois says.

The team is seeking to expand our understanding of the neurological correlates of dissociation in order to clarify historical misunderstandings about dissociation and DID, destigmatize these experiences, and help to lessening gender-related health inequalities.
“We also hope that it will raise awareness of dissociative symptoms,” said co-senior author Milissa Kaufman, MD, PhD, head of the Dissociative Disorders and Trauma Research Program.
According to the study’s authors, the different brain fingerprints of the various dissociative disorders may highlight the need for innovative therapies.

According to co-author Kerry J. Ressler, MD, PhD, chief scientific officer for McLean, future study may focus on dissociation-related brain activity as a solo treatment.

McLean Hospital, the biggest psychiatric affiliate of Harvard Medical School and a component of Mass General Brigham, has uncovered locations within brain networks that communicate with one another when persons suffer dissociative symptoms. Their findings were published in the journal Neuropsychopharmacology recently.

Trauma can cause dissociative symptoms such as out-of-body experiences or emotional numbness, which can be useful in the short term but dangerous if they persist over an extended period of time.

“Dissociation and severe dissociative disorders like dissociative identity disorder or ‘DID’ remain at best underappreciated and, at worst, frequently go undiagnosed or misdiagnosed,” said co-lead author Lauren A.M. Lebois, PhD, director of the Dissociative Disorders and Trauma Research Program.

“The cost of this stigmatization and misdiagnosis is high–it has prevented people from accessing appropriate and effective treatment, caused prolonged suffering, and stunted research on dissociation. In addition, given that DID disproportionately affect women, gender disparity is an important issue in this context.”

91 women with and without histories of childhood trauma, current post-traumatic stress disorder, and varying degrees of dissociative symptoms participated in Lebois and colleagues’ study. A functional magnetic resonance imaging scan was done by participants so that researchers could learn more about their brain activity.

“The novel methods we used to study brain connectivity are critical for understanding the role these network disturbances play in dissociative disorders,” said co-senior author Lisa D. Nickerson, PhD, director of the Applied Neuroimaging Statistics Lab at McLean Hospital.

The researchers discovered that specific connections between regions in the brain networks that control cognition and emotional processes were connected with certain dissociation symptoms. According to Lebois, “We discovered that dissociation key to DID and dissociation common to post-traumatic stress disorder are each linked to specific brain signatures.”

In order to correct historical misconceptions regarding dissociation and DID, destigmatize these experiences, and contribute to lowering gender-related health disparities, the team is working to improve our understanding of the neural correlates of dissociation.

“We also hope it will increase awareness of dissociative symptoms–and that, ultimately, clinicians will be more likely to assess for and consider these symptoms, and to connect patients with timely and appropriate treatment,” said co-senior author Milissa Kaufman, MD, PhD, director of the Dissociative Disorders and Trauma Research Program.

It is significant to note that the various dissociative disorders’ distinct brain signatures may indicate the need for novel treatments, according to the study’s authors. Future research may focus on dissociation-related brain activity as a standalone treatment, according to co-author Kerry J. Ressler, MD, PhD, chief scientific officer for McLean.